The patient is a 72-year-old man with a history of ischemic cardiomyopathy (LV ejection fraction, 30%\u201335%) and NYHA class II\/III heart-failure symptoms at baseline. Over the previous month, he had experienced recurrent episodes of volume overload and sustained ventricular tachycardia (VT) requiring intravenous diuretics and up-titration of his amiodarone therapy. He then presented in VT storm, requiring intravenous lidocaine in addition to amiodarone, and was transferred to a tertiary care facility for potential VT ablation.<\/p>\n
His additional medical history is noteworthy for hypertension, hyperlipidemia, insulin-dependent type II diabetes mellitus, paroxysmal atrial fibrillation, chronic renal insufficiency (serum creatinine, 1.5 mg\/dL), mild chronic obstructive lung disease, and Parkinson’s disease. He underwent bypass surgery for coronary atherosclerosis in 2004 and received a biventricular pacemaker\/defibrillator in 2005.<\/p>\n
At the tertiary facility, an echocardiogram revealed an LVEF of 30%\u201335% (LV end-diastolic diameter, 5.1 cm) with global hypokinesis. Moderate-to-severe RV dysfunction was identified. The patient had a heavily calcified, trileaflet aortic valve with a peak gradient of 29 mm Hg, a mean gradient of 18 mm Hg, and a calculated valve area of 0.6 cm2. He also had moderate mitral regurgitation (regurgitant volume, 52 mL). His estimated pulmonary-artery systolic pressure was 21 mm Hg + RA.<\/p>\n
A subsequent catheterization confirmed severe aortic stenosis and revealed native 3-vessel disease with patent grafts. A FDG-PET scan showed a small area of inferior scar but no ischemia.<\/p>\n
Questions:<\/strong><\/p>\n <\/p>\n This man appears to have significant aortic stenosis despite his modest gradient. Although the cath lab findings are not reported, they appear to corroborate the echocardiographic findings. No comment is made of assessing contractile reserve, which would help to rule out pseudo-aortic stenosis; this assessment can be done either in the cath lab or using echocardiography. Assuming that such an assessment would confirm severe aortic stenosis, I would recommend surgical aortic valve replacement.<\/p>\n Two other issues should also be resolved before surgery is entertained. The presence of a \u201cporcelain\u201d aorta would temper the enthusiasm for surgical AVR. In addition, the moderate-to-severe RV dysfunction is of concern and needs to be further clarified in the cath lab. The CVP, RVSWI, and TR are not commented on. This degree of RV dysfunction is not typically seen with severe aortic stenosis.<\/p>\n The patient\u2019s comorbidities and the redo nature of an AVR increase his operative mortality. Based on publicly available risk scoring tools, his predicted mortality is in the range of 9% (STS) to 25% (EuroScore). Although these scores have been validated in various populations, they appear, to many clinicians, to overestimate risk in clinical practice. This issue has limited the interpretation of the published TAVI experience, and we await large randomized (albeit not blinded) studies such as PARTNER.<\/p>\n If surgical expertise is not available, a percutaneous AVR could be offered as an alternative but should be done in the context of a clinical trial. The durability of percutaneous valves is not clear and cannot be compared to conventional AVR in this regard at this time. Certainly, the recently published\u00a0Canadian experience<\/a> (with both transapical and transfemoral approaches) is encouraging. A \u201cbridging\u201d strategy could include valvuloplasty, with the understanding that the results would be temporary; this approach would primarily serve to reassure the clinicians that AVR of any sort is worth undertaking, while also potentially improving the baseline hemodynamic status of the patient.<\/p>\n There is reasonable evidence that wall stress and decompensated heart failure are arrhythmogenic; the patient\u2019s aortic stenosis appears to be significant enough to contribute to this scenario. It would also be important to assess his CRT. LV stimulation can be pro-arrhythmic in certain substrates \u2014 particularly in ischemic heart disease, due to the nature of the scarring involved.<\/p>\n Follow-Up:<\/strong><\/p>\n The patient underwent aortic valve replacement with a bioprosthetic valve.\u00a0The total bypass time was 224 minutes with a cross clamp time of 114 minutes.\u00a0On post-operative day 2, the patient was successfully weaned off pressor and intra-aortic balloon pump support. However, he was massively volume overloaded and remained somnolent, despite lack of sedation, making extubation difficult. An attempt at diuresis with escalating doses of intravenous furosemide was unsuccessful.\u00a0CVVH was started but diuresis was limited by fever and hypotension.\u00a0In this context,\u00a0the patient\u00a0developed recurrent ventricular tachycardias, requiring anti-tachycardia pacing by his device.\u00a0Due to the\u00a0his continued ventilator dependence, a tracheostomy and percutaneous endoscopic gastrostomy tube were placed on post-operative day 12.\u00a0A chest CT revealed multifocal pneumonia and the patient was treated with broad spectrum antibiotics.\u00a0He developed a spontaneous pneumothorax, requiring chest tube placement.\u00a0He then developed progressive hypotension with evidence of Staphylococcus aureus bactermia.\u00a0Despite escalating support, the patient suffered an asystolic arrest and\u00a0died on post-operative day 20.<\/p>\n\n
\nResponse:
\n<\/strong>James Fang, MD<\/strong><\/a><\/p>\n